| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10738264 | Free Radical Biology and Medicine | 2012 | 11 Pages |
Abstract
⺠NASH pathogenesis is widely recognized as a two-hit model. ⺠The “first hit” is an initial metabolic disturbance increasing inflow of free fats. ⺠The “second hit” includes oxidative stress, decreased hepatic ATP and inflammation. ⺠Impaired mitochondrial bioenergetics, function and morphology are observed.
Keywords
MCDGSHFFAGPXOXPHOSHO-1NRFAMPKRNSPPARPGC-1αHNETFAMHeme oxygenase-1ANTUCP-2NRTICYP2E1ChREBPCPT-1ACC1ΔpHMDATGF-βNAFLDcarbohydrate responsive element-binding proteinmethionine- and choline-deficient dietTCASREBP-1cHSCFAS4-hydroxy-2-nonenalAMP-activated protein kinaseCDDMitochondrial DNAROSS-adenosylmethioninenonalcoholic steatohepatitisacetyl-CoA carboxylase 1tricarboxylic acidFree fatty acidfatty acid synthasePolyunsaturated fatty acidPUFAFatty acidsinflammationOxidationinterleukinNonalcoholic fatty liver diseasetransforming growth factor-βadenine nucleotide translocatorOxidative stresstumor necrosis factor-αmtDNAFree radicalscholine-deficient dietelectron transport chainHepatic stellate cellCytochrome P450CytokinesNuclear respiratory factorTNF-αOxidative phosphorylationUncoupling Protein-2malondialdehydeMitochondriaNash ETcMitochondrial membrane potentialsterol regulatory element-binding protein-1cCarnitine palmitoyltransferase 1Glutathioneglutathione peroxidasereactive nitrogen speciesReactive oxygen speciesperoxisome proliferator-activated receptorSAMe
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Authors
Anabela P. Rolo, João S. Teodoro, Carlos M. Palmeira,